Evidence map›Paper›PMID 20032512›Full record

ArticleAmerican journal of physiology. Cell physiology2010

CYP1B1 and endothelial nitric oxide synthase combine to sustain proangiogenic functions of endothelial cells under hyperoxic stress.

Yixin Tang, Elizabeth A Scheef, Zafer Gurel, Christine M Sorenson, Colin R Jefcoate, Nader Sheibani

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.1field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
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  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. The role of cytochrome P450 (CYP) enzymes in hyperoxic lung injury.Expert opinion on drug metabolism & toxicology · 2021
    Review
  13. CYP1B1 as a therapeutic target in cardio-oncology.Clinical science (London, England : 1979) · 2020
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Mice Lacking the Cytochrome P450 1B1 Gene Are Less Susceptible to Hyperoxic Lung Injury Than Wild Type.Toxicological sciences : an official journal of the Society of Toxicology · 2018
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Yixin TangUniv. of Wisconsin, Dept. of Ophthalmology and Visual Sciences, 600 Highland Ave., K6458 CSC, Madison, WI 53792-4673, USA.
Elizabeth A Scheef
Zafer Gurel
Christine M Sorenson
Colin R Jefcoate
Nader Sheibani
University of Wisconsin–Madison · USPediatrics and Genetics · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI ROBERT W NICKELLS · 2005 to 2026
$12.6M
Bcl-2 &Branching MorphogenesisR01DK067120 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI SORENSON, CHRISTINE M · 2005 to 2008
$1.1M
CYP1B1 and Retinopathy of PrematurityR01EY018179 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI SHEIBANI, NADER · 2009 to 2010
$713k
MECHANISMS OF DMBA INDUCED BONE MARROW TOXICITYR01CA081493 · NCI · UNIVERSITY OF WISCONSIN MADISON · PI CZUPRYNSKI, CHARLES J · 1999 to 2002
$629k
NCI NIH HHS CA-81493NCI NIH HHS P30 CA-014520NEI NIH HHS EY-16995NEI NIH HHS EY-18179NEI NIH HHS P30 EY016665NEI NIH HHS P30 EY-16665NIDDK NIH HHS DK-67120
6 · The paper itself

Abstract

We have recently shown that deletion of constitutively expressed CYP1B1 is associated with attenuation of retinal endothelial cell (EC) capillary morphogenesis (CM) in vitro and angiogenesis in vivo. This was largely caused by increased intracellular oxidative stress and increased production of thrombospondin-2, an endogenous inhibitor of angiogenesis. Here, we demonstrate that endothelium nitric oxide synthase (eNOS) expression is dramatically decreased in the ECs prepared from retina, lung, heart, and aorta of CYP1B1-deficient (CYP1B1(-/-)) mice compared with wild-type (CYP1B1(+/+)) mice. The eNOS expression was also decreased in retinal vasculature of CYP1B1(-/-) mice. Inhibition of eNOS activity in cultured CYP1B1(+/+) retinal ECs blocked CM and was concomitant with increased oxidative stress, like in CYP1B1(-/-) retinal ECs. In addition, expression of eNOS in CYP1B1(-/-) retinal ECs or their incubation with a nitric oxide (NO) donor enhanced NO levels, lowered oxidative stress, and improved cell migration and CM. Inhibition of CYP1B1 activity in the CYP1B1(+/+) retinal ECs resulted in reduced NO levels and attenuation of CM. In contrast, expression of CYP1B1 increased NO levels and enhanced CM of CYP1B1(-/-) retinal ECs. Furthermore, attenuation of CYP1B1 expression with small interfering RNA proportionally lowered eNOS expression and NO levels in wild-type cells. Together, our results link CYP1B1 metabolism in retinal ECs with sustained eNOS activity and NO synthesis and/or bioavailability and low oxidative stress and thrombospondin-2 expression. Thus CYP1B1 and eNOS cooperate in different ways to lower oxidative stress and thereby to promote CM in vitro and angiogenesis in vivo.

Indexed as

Neovascularization, PhysiologicOxidative StressAdenoviridaeAnimalsAntioxidantsAortaAryl Hydrocarbon HydroxylasesCell LineCell MovementCoronary VesselsCytochrome P-450 CYP1B1Endothelial CellsEnzyme InhibitorsGenetic VectorsGenotypeHumansAntioxidantsAryl Hydrocarbon HydroxylasesCYP1B1 protein, humanCyp1b1 protein, mouseCytochrome P-450 CYP1B1Enzyme InhibitorsNitric OxideNitric Oxide DonorsNitric Oxide Synthase Type IIINos3 protein, mouseReactive Oxygen SpeciesThrombospondin 2Thrombospondins

Identifiers

PMID20032512
PMCPMC2838582
OpenAlexW1994276651

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.